Probably not a good idea to take an antipsychotic drug for anxiety/insomnia. You may have difficulty withdrawing from this drug.
Not sure if I should start a new thread but a few times now, people on the Abilify FB group have mentioned using Avena sativa instead of Abilify.
Has anyone heard about this and/or tried it?
That's s huuuuuuuge leap. Abilify vs. oats?people on the Abilify FB group have mentioned using Avena sativa instead of Abilify.
That's s huuuuuuuge leap. Abilify vs. oats?
What form of oats? Extract? Seed? Stems?
I'd say definitely start a new thread. This is really interesting, but Im not too clear on oats vs. a strong anti-psychotic drug ....
Thank yo for posting a link .... it's a fascinating possibility, and deserves more attention than it would get buried here in a thread about Stanford and Abilify research .....
Yes, for these third generation antipsychotics like amisulpride and aripiprazole, these drugs are classed as dopamine system stabilizers, which means the drug acts as an agonist of the dopamine receptors at low dopamine concentrations, but acts as an antagonist at high dopamine concentrations.
So these drugs boost the dopamine system when dopamine is low, but put the breaks on the dopamine system when dopamine is high. Refs: 1 2
The response to amisulpride is also dose-level dependent:
At low doses, amisulpride blocks the dopamine autoreceptors. An autoreceptor is presynaptic regulatory feedback mechanism which controls how much of a neurotransmitter like dopamine is being released into the synapse (the junction between neurons). When you block the dopamine autoreceptors, it makes the neuron think there is not enough dopamine in the synapse, so more dopamine is released. In this way, blocking dopamine autoreceptors leads to more dopamine release.
But at high doses of amisulpride, then this drug starts to antagonize the postsynaptic dopamine receptor (the normal dopamine receptor), and at these higher doses the overall effect is dopamine antagonism. Refs: 1 2
Aripiprazole behaves similarly at the presynaptic and postsynaptic dopamine receptors. This paper says:
Some more info in the first post of this thread.
If we look at D3 receptors, the action of Aripiprazole on them produces a pro-cognitive effect. Action on D2 receptors means 90% binding, and binding to D3 receptors is also 90%. The clinical correspondent is increasing motivation and preventing diabetes (in a class of medicines where most are at risk of producing diabetes)
Yes, this would be nice, wouldn't it? It still won't fix thyroid hormone imbalances, adrenal insufficiency, lack of testosterone or other sex hormones, B vitamin deficiencies amino acid deficiencies, lack of minerals, active Epstein-Barr or other herpes virus or other viral or bacterial infections, autoimmune processes, hypercoagulation, spinal issues, mast cell activation, and whatever else patients have going on.
I have spoken at length with Robert Naviaux, and he suggested that removing all the cell dangers on his list of categories of things that provoke cell danger response and then moving from winter metabolism to summer metabolism should be helpful, and then only if normal function is not restored, then one would try suramin.
I did, six months. It just never worked again. I gave up on abilify.Hmnr, I think I recall you saying that you'll take a break and retry, did you do that
I did, six months. It just never worked again. I gave up on abilify.
I'm doing pretty bad right now. Thinking of starting a course of antibiotics ( just a shot in the dark, not hoping for much).
PS I can't believe you read the whole thread!